Radiation carcinogenesis modelling for risk of treatment-related second tumours following radiotherapy

Radiobiological modelling of the risk of radiation-induced tumours followin g high dose radiation implies a general form for the dose-response relation ship. Generally, risk will rise with radiation dose at low doses, reach a m aximum value and then decline with further increase in dose. The magnitude of risk and the dose at which this risk is maximum are strongly dependent o n the kinetics of repopulation by surviving normal and mutant cells and on genetic factors likely to differ between tissues and between individuals. T he most reliable way to reduce the risk of second tumours is to reduce radi ation dose further at sites where the dose is already low. These sites are usually distant from the primary treatment volume. For illustrative purpose s, we have compared the predicted relative risks of second tumours at "dist ant sites" for treatment plans giving similar dose distributions (dose volu me histograms) at the primary site. We suggest that dose reduction to dista nt sites could be of significant benefit in reducing the risk of second tum ours. Further improvement will require more detailed knowledge of the radia tion sensitivities and mutagenicities, together with the repopulation kinet ics of the various cell lineages within the treatment volume.